Positron Emission-Computed Tomography, Cryobiopsy versus Bronchoalveolar Lavage and Computed Tomography Findings for Interstitial Lung Disease: A Long-Term Follow-Up.

Background and Objectives: Interstitial lung diseases have always been an issue for pulmonary and rheumatology physicians. Computed tomography scans with a high-resolution protocol and bronchoalveolar lavage have been used along with biochemical blood tests to reach a diagnosis. Materials and Methods: We included 80 patients in total. First, all patients had their diagnosis with computed tomography of the thorax, serological/ immunological blood tests and bronchoalveolar lavage. However; after 3 months, all were divided into 2 groups: those who had bronchoalveolar lavage again and those who had cryobiopsy instead of bronchoalveolar lavage (40/40). Positron emission-computed tomography was also performed upon the first and second diagnosis. The patients' follow-up was 4 years from diagnosis. Results: Patients suffered most from chronic obstructive pulmonary disease (56, 70%), while lung cancer was rarely encountered in the sample (7, 9.75%). Age distribution ranged between 53 and 68 years with a mean value of 60 years. The computed tomography findings revealed 25 patients with typical diagnosis (35.2%), 17 with interstitial pulmonary fibrosis (23.9%) and 11 with probable diagnosis (11%). The cryobiopsy technique led to a new diagnosis in 28 patients (35% of the total sample). Patients who had a new diagnosis with cryobiopsy had a mean survival time of 710 days (<1460). Positron emission-computed tomography SUV uptake was positively associated with the cryobiopsy technique/new disease diagnosis and improved all respiratory functions. Discussion: Positron emission-computed tomography is a tool that can be used along with respiratory functions for disease evaluation. Conclusions: Cryobiopsy is a safe tool for patients with interstitial lung disease and can assist in the diagnosis of interstitial lung diseases. The survival of patients was increased in the cryobiopsy group versus only bronchoalveolar lavage for disease diagnosis.

Halomonas binhaiensis sp. nov., isolated from saline-alkali soil.

A Gram-stain-negative, aerobic and rod-shaped bacterium, strain Y2R2T, was isolated from a saline-alkali soil sample collected from Binhai New Area, Tianjin, PR China. Growth of strain Y2R2T was observed at 10-45 °C (optimum, 30 °C), at pH 6.0-11.0 (optimum, pH 9.0) and in the presence of 0-15 % (w/v) NaCl (optimum, 9.0 %). Phylogenetic analysis based on 16S rRNA gene sequences showed that strain Y2R2T was affiliated with the genus Halomonas and showed the highest similarity to Halomonas huangheensis BJGMM-B45T (99.0%) and Halomonas cupida DSM 4740T (98.4%). The digital DNA-DNA hybridization and average nucleotide identity values of 21.0-22.8 % and 73.3-75.7 % with the closely related species H. huangheensis BJGMM-B45T, H. cupida DSM 4740T, H. ventosae AL12T, H. stenophila N12T and H. litopenaei SYSU ZJ2214T were lower than the threshold recommended for species discrimination.The major respiratory quinone of strain Y2R2T was Q-9 and the major cellular fatty acids consisted of C16 : 0, C19 : 0 cyclo ω8c and summed feature 8 (C18 : 1 ω7c and/or C18 : 1 ω6c). The DNA G+C content of strain Y2R2T was 57.0 mol%. On the basis of this polyphasic taxonomic study, strain Y2R2T is considered to represent a novel species of the genus Halomonas, for which the name Halomonas binhaiensis sp. nov. is proposed. The type strain is Y2R2T (=CGMCC 1.16974T=KCTC 72578T).

Treg-dependent immunosuppression triggers effector T cell dysfunction via the STING/ILC2 axis.

Lung cancer remains the leading cause of cancer-related deaths and despite extensive research, the survival rate of lung cancer patients remains significantly low. Recent data reveal that aberrant Kras signaling drives regulatory T cells (Tregs) present in lung tumor microenvironment to establish immune deregulation and immunosuppression but the exact pathogenic mechanism is still unknown. In this study, we investigate the role of oncogenic Kras in Treg-related immunosuppression and its involvement in tumor-associated metabolic reprogramming. Findings reveal Tregs to prompt GATA3/NOS2-related immunosuppression via STING inhibition which triggers a decline in CD4+ T infiltration, and a subsequent increase in lung metastatic burden. Enhanced Treg expression was also associated with low T/MDSC ratio through restriction of CD8+CD44+CD62L- T effector cells, contributing to a tumor-promoting status. Specifically, TIM3+/LAG3+ Tregs prompted Kras-related immunosuppressive chemoresistance and were associated with T cell dysfunction. This Treg-dependent immunosuppression correlated with CD8 T cell exhaustion phenotype and ILC2 augmentation in mice. Moreover, enhanced Treg expression promoted activation-induced cell death (AICD) of T lymphocytes and guided lymph node metastasis in vivo. Overall, these findings demonstrate the multifaceted roles of Tregs in sustaining lung immunosuppressive neoplasia through tumor microenvironment remodeling and provide new opportunities for effective metastasis inhibition, especially in chemoresistant tumors.

Mutagenic Effects of a 2-Deoxyribonolactone-Thymine Glycol Tandem DNA Lesion in Human Cells.

Tandem DNA lesions containing two contiguously damaged nucleotides are commonly formed by ionizing radiation. Their effects on replication in mammalian cells are largely unknown. Replication of isolated 2-deoxyribonolactone (L), thymine glycol (Tg), and tandem lesion 5'-LTg was examined in human cells. Although nearly 100% of Tg was bypassed in HEK 293T cells, L was a significant replication block. 5'-LTg was an even stronger replication block with 5% TLS efficiency. The mutation frequency (MF) of Tg was 3.4%, which increased to 3.9% and 4.8% in pol ι- and pol κ-deficient cells, respectively. An even greater increase in the MF of Tg (to ∼5.5%) was observed in cells deficient in both pol κ and pol ζ, suggesting that they work together to bypass Tg in an error-free manner. Isolated L bypass generated 12-18% one-base deletions, which increased as much as 60% in TLS polymerase-deficient cells. The fraction of deletion products also increased in TLS polymerase-deficient cells upon 5'-LTg bypass. In full-length products and in all cell types, dA was preferentially incorporated opposite an isolated L as well as when it was part of a tandem lesion. However, misincorporation opposite Tg increased significantly when it was part of a tandem lesion. In wild type cells, targeted mutations increased about 3-fold to 9.7% and to 17.4, 15.9, and 28.8% in pol κ-, pol ζ-, and pol ι-deficient cells, respectively. Overall, Tg is significantly more miscoding as part of a tandem lesion, and error-free Tg replication in HEK 293T cells requires participation of the TLS polymerases.

The histone demethylase JMJD2A promotes glioma cell growth via targeting Akt-mTOR signaling.

BACKGROUND: A number of JmjC domain-containing histone demethylases have been identified and biochemically characterized in mammalian models and humans. JMJD2A is a transcriptional co-factor and enzyme that catalyzes the demethylation of histone H3 lysine 9 and 36 (H3K9 and H3K36). Here in this study, we reported the role of JMJD2A in human glioma. METHODS: Quantitative real-time PCR and western blot were performed to analyzed JMJD2A expression in glioma. Log-rank was performed to plot the survival curve. JMJD2A was knocked or overexpressed with lentivirus. Cell proliferation and colony formation were performed to assess the effects of JMJD2A on glioma cell growth. Xenograft experiment was performed the evaluate the growth rate of glioma cells in vivo. The signaling pathway was analyzed with western blot and mTOR was inhibited with rapamycin. RESULTS: Quantitative real-time PCR and western blot experiments revealed higher expression of JMJD2A and lower levels of H3K9me3/H3K36me3 in glioma tissues than that in normal brain tissues. We showed that knockdown of JMJD2A expression attenuated the growth and colony formation in three lines of glioma cells (U251, T98G, and U87MG), whereas JMJD2A overexpression resulted in opposing effects. Furthermore, we performed in vivo xenograft experiments and our data demonstrated that JMJD2A knockdown reduced the growth of glioma T98G cells in vivo. Further mechanism study implicated that JMJD2A activated the Akt-mTOR pathway and promoted protein synthesis in glioma cells via promoting phosphoinositide-dependent kinase-1 (PDK1) expression. The activation of the Akt-mTOR pathway was also validated in human glioma tissues. Finally, we showed that inhibition of mTOR with rapamycin blocked the effects of JMJD2A on protein synthesis, cell proliferation and colony formation of glioma cells. CONCLUSIONS: These findings demonstrated that JMJD2A regulated glioma growth and implicated that JMJD2A might be a promising target for intervention.

Interventional Bronchoscopy for the Treatment of Malignant Central Airway Stenosis: An Expert Recommendation for China.

Malignant central airway stenosis refers to airway stenosis caused by primary or metastatic malignant tumors which may lead to different levels of dyspnea or asphyxia in patients. With the rapid development of interventional pulmonology, therapeutic bronchoscopy has become one of the main methods for the diagnosis and treatment of malignant central airway stenosis. However, the level of diagnosis and treatment of respiratory intervention techniques in China is uneven at present, the treatment methods are not uniform, the treatment effects vary greatly, and some treatments even lead to serious complications. The interventional treatment technology for malignant central airway stenosis in China needs to be standardized. Therefore, the relevant experts of the Beijing Health Promotion Association Respiratory and Oncology Intervention and Treatment Alliance have formulated this consensus after several rounds of full discussion.

Massilia armeniaca sp. nov., isolated from desert soil.

A Gram-stain-negative, aerobic, motile and rod-shaped bacterium, strain ZMN-3T, was isolated from desert soil sample collected from Ongniod Qi, Inner Mongolia, China. Phylogenetic analysis based on 16S rRNA gene sequences showed that strain ZMN-3T was affiliated with the genus Massilia and showed the highest similarity to Massilia humi THG S6-8T (98.9 %) and Massilia buxea A9T (98.2 %). In partial gyrB and lepA sequences, the highest similarity of strain ZMN-3T and M. humi THG S6-8T were 95.9 and 96.8 %, respectively. The DNA-DNA hybridization value between strain ZMN-3T and its closely related type strains were all below 70 %. The major respiratory quinone of strain ZMN-3T was Q-8 and the major cellular fatty acids consisted of summed feature 3 (C16 : 1ω7c and/or C16 : 1ω6c) and C16 : 0. The predominant polar lipids contained diphosphatidylglycerol, phosphatidylglycerol, phosphatidylethanolamine and an unidentified phospholipid. The DNA G+C content of strain ZMN-3T was 66.3 mol%. On the basis of this polyphasic taxonomic study, strain ZMN-3T is considered to represent a novel species of the genus Massilia, for which the name Massilia armeniaca sp. nov. is proposed. The type strain is ZMN-3T (=CGMCC 1.16209T=DSM 104676T).

Sleep disorders and health-related quality of life in patients with interstitial lung disease.

BACKGROUND: Interstitial lung diseases (ILD) are chronic and restrictive lung diseases with poor survival and quality of life. The aim of this study was to investigate the frequency of sleep disorders in idiopathic pulmonary fibrosis (IPF) and sarcoidosis and to assess patients' quality of life in relation to these disorders. METHODS: Forty patients, 19 with IPF, and 21 with sarcoidosis stage II/III were included. They were compared with 15 healthy subjects. All patients performed all-night polysomnography (PSG) and completed the Epworth, Berlin, and Stop-Bang questionnaires. In order to evaluate the quality of life, all patients completed the Short-Form 36 (SF-36) questionnaire. RESULTS: Of the IPF patients, 68% were diagnosed with mild obstructive sleep apnea (OSA), 5.2% with moderate to severe, 5.2% with severe OSA, and 21% with no OSA. Of patients with sarcoidosis, 52.4% were diagnosed with mild OSA and 4.8% with moderate severity OSA. The remaining 42.8% did not have OSA. The health-related quality of life in both patients with IPF and patients with sarcoidosis was impaired especially in the domains concerning physical health and the level of independence, compared to the control group. CONCLUSIONS: In this sample of patients with IPF and sarcoidosis, obstructive sleep apnea is common at least in a mild degree of severity. The SF-36 questionnaire may be a useful tool for the evaluation of the quality of life in these patients.

Low-frequency band gap of locally resonant phononic crystals with a dual-base plate.

To achieve a wider band gap and a lower cut-on frequency, a locally resonant phononic crystal (LRPC) with a dual-base plate is investigated in this paper. Compared with the LRPC with a single plate, the band structure of the LRPC with a dual-base plate is calculated using the method of plane wave expansion and verified by the finite element method. According to the analysis of the band curves of the LRPC with a dual-base plate, the mechanisms are explained. Next, the influences of the thickness of the plates, the stiffness of the springs, the mass of resonators, and the lattice constant are also investigated. The results show that the structural asymmetry between the upper and the lower plate is conducive to reducing the cut-on frequency and broadening the band gap effectively. The results indicate a different approach for the application of LRPC in vibration and noise control.

Upregulated expression of Nogo-A and NgR in an experimental model of focal microgyria regulates the migration, proliferation and self-renewal of subventricular zone neural progenitors.

Nogo-A and its receptor (NgR) were first described as myelin-associated inhibitors of neuronal regeneration in response to injury. In recent years, knowledge about the important role of the Nogo-A protein in several neuronal pathologies has grown considerably. Here, we employed a neonatal cortex freeze-lesion (NFL) model in neonatal rats and measured the expression of Nogo-A and NgR in the resulting cerebrocortical microdysgenesis 5-75 days after freezing injury. We observed marked upregulation of Nogo-A and NgR in protein levels. Furthermore, the migration of neural precursor cells (NPCs) derived from the subventricular zone (SVZ) toward the sits of injury was perturbed by treatment of NgR antagonist peptide NEP1-40. In vitro analysis showed that the knockdown of NgR by lentivirus-delivered siRNA promoted in axonal regeneration and SVZ-derived neural stem cell/progenitor cell (SVZ-NPCs) adhesion and migration, findings which were similar to the effects of NEP1-40. Taken together, our results indicate an important role for NgR in regulating the physiological processes of SVZ-NPCs. The observation of upregulated Nogo-A/NgR in lesion sites in the NFL model suggest that the effects of the perturbed Nogo-A are a key feature during the development and/or the progression of cortical malformation.

Myocyte enhancer factor 2D promotes tumorigenicity in malignant glioma cells.

The prognosis of patients with malignant glioma is always quite poor, and this poor prognosis is probably due to our incomplete understanding of the molecular mechanisms underlying malignant glioma. It is known that myocyte enhancer factor-2D (MEF2D) plays an oncogenic role in hepatocellular carcinoma and promotes the survival of various types of cells. However, little is known about the expression profile and function of MEF2D in malignant glioma. In this study, we investigated the function and expression of MEF2D in malignant glioma. We found that in malignant glioma, there is an aberrantly high expression of MEF2D, which leads to poor prognosis of malignant glioma. The downregulation of MEF2D suppresses the proliferation of malignant glioma cell lines by inducing delay of S and G2/M phases of cell cycle and promoting apoptosis. Furthermore, the overexpression of MEF2D in astrocytes accelerates cell proliferation by regulating cell cycle progression. Furthermore, a mouse malignant glioma model demonstrated that MEF2D deficiency blocks malignant glioma formation in vivo. We conclude that MEF2D may act as a potential oncogene in malignant glioma and thus serve as a candidate target for malignant glioma therapy.

Synthesis of N7-Alkyl-9-deaza-2'-deoxyguanosines Containing Polar N7 Chains. Examples of Chemically Stable Analogues of N7-Hydroxyethyl and N7-Oxoethyl Adducts of 2'-Deoxyguanosine.

Development of chemically stable analogues of unstable DNA lesions enables accurate study of polymerase bypass. We report the design and synthesis of N7-hydroxyethyl-9-deaza-2'-deoxyguanosine and N7-oxoethyl-9-deaza-2'-deoxyguanosine as the analogues of N7-hydroxyethyl-2'-deoxyguanosine and N7-oxoethyl-2'-deoxyguanosine, respectively. We also developed the synthesis of these two nucleosides whose N7 side chains are protected by TBS for the convenience of conversion to phosphoramidites.

Flexible bronchoscopy-induced massive bleeding: A 12-year multicentre retrospective cohort study.

BACKGROUND AND OBJECTIVE: Although massive bleeding is the most life-threatening complication caused by flexible bronchoscopy, data on flexible bronchoscopy-induced massive bleeding are scarce, and the associated clinical characteristics and prognostic factors are unknown. METHODS: This was a multicentre retrospective cohort study of all patients who underwent flexible bronchoscopy in 33 tertiary hospitals from January 2001 to June 2013. The clinical characteristics and outcomes were collected and analysed. RESULTS: A total of 194 patients with massive bleeding were identified among 520 343 patients who underwent flexible bronchoscopy. The average blood loss reached up to 378 mL. The overall incidence and mortality were 0.037% and 0.004%, respectively, and the overall fatality was 10.8%. The risk of massive bleeding induced by therapeutic bronchoscopies was significantly higher than that induced by diagnostic bronchoscopies (incidence: 0.059% vs 0.031%, P < 0.001; mortality: 0.012% vs 0.003%, P < 0.001; fatality: 20% vs 8.4%, P = 0.068). Multivariate analysis showed that age ≥65 years, tracheal bleeding, blood loss ≥500 mL and occurrence of shock were independent factors predicting poor outcome, while emergency surgery was an independent protective factor. Re-bleeding occurred in six patients, resulting in three deaths within a month. CONCLUSION: Flexible bronchoscopy-induced massive bleeding is rare but life-threatening. Age, bleeding location, bleeding volume, circulation condition and emergency surgery were independent prognostic factors.

Highly specific colorimetric detection of DNA oxidation biomarker using gold nanoparticle/triplex DNA conjugates.

DNA oxidation causes a variety of diseases including cancer. The oxidized DNA nucleobases are excised by cellular repair enzymes and released into extracellular fluids. Specifically, the excised DNA oxidation product, such as 8-oxoGua, has been suggested as a biomarker for early cancer diagnosis. We previously developed an artificial receptor for the free base of 8-oxoGua on a triplex DNA backbone. The receptor contained a pre-organized cavity, which bounded 8-oxoGua with strong affinity and excellent selectivity over other nucleobases. However, accurate detection of 8-oxoGua in urine samples was affected by the presence of a large excess of guanine. Herein, we report a strategy to convert our receptor to a colorimetric biosensor by conjugating DNA strands to gold nanoparticles (GNP), specifically for 8-oxoGua. By simply incubating our sensor with a urine sample, 8-oxoGua can be detected at submicromolar concentrations with UV-vis spectrometer or even by naked eye.

Molecular recognition of pyrimidine nucleobases by triplex DNA receptors.

Triplex DNA receptors are known for their strong and specific binding of a variety of purine ligands. However, not many studies have been reported on their binding of pyrimidine ligands. Here we used fluorophore-labeled DNA receptors to study these binding interactions. The results suggest that in general, cytosine binds more strongly than thymine and uracil, although the selectivity between two pyrimidine ligands can be tuned by changing the surrounding nucleobases of the DNA receptor. In contrast, binding of pyrimidine nucleosides is much weaker, possibly due to lack of the N1 hydrogen bonding donor.

Proteomic comparison of 3D and 2D glioma models reveals increased HLA-E expression in 3D models is associated with resistance to NK cell-mediated cytotoxicity.

Three-dimensional cell culture techniques can better reflect the in vivo characteristics of tumor cells compared with traditional monolayer cultures. Compared with their 2D counterparts, 3D-cultured tumor cells showed enhanced resistance to the cytotoxic T cell-mediated immune response. However, it remains unclear whether 3D-cultured tumor cells have an enhanced resistance to NK cell cytotoxicity. In this study, a total of 363 differentially expressed proteins were identified between the 2D- and 3D-cultured U251 cells by comparative proteomics, and an immune-associated protein-protein interaction (PPI) network based on these differential proteins was constructed by bioinformatics. Within the network, HLA-E, as a molecule for inhibiting NK cell activation, was significantly up-regulated in the 3D-cultured tumor cells. Then, we found that the 3D-cultured U251 cells exhibited potent resistance to NK cell cytotoxicity in vitro and were prone to tumor formation in vivo. The resistance of the 3D-cultured tumor cells to NK cell lysis was mediated by the HLA-E/NKG2A interaction because the administration of antibodies that block either HLA-E or NKG2A completely eliminated this resistance and significantly decreased tumor formation. Taken together, our findings indicate that HLA-E up-regulation in 3D-cultured cells may result in enhanced tumor resistance to NK cell-mediated immune response.

Overexpression of MACC1 protein and its clinical implications in patients with glioma.

Metastasis associated in colon cancer 1 (MACC1) has been regarded as a novel potential therapeutic target for multiple cancers. However, the impact of MACC1 in glioma remains unclear. The aim of this study was to analyze the correlation of MACC1 expression with the clinicopathological features of glioma. MACC1 mRNA and protein expression levels in human glioma tissues were detected by quantitative real-time polymerase chain reaction and immunohistochemistry assays, respectively. MACC1 mRNA and protein expression were both significantly higher in glioma tissues than in corresponding noncancerous brain tissues (both P < 0.001). In addition, statistical analysis suggested that high MACC1 expression was significantly correlated with advanced pathological grade (P = 0.004) and that patients with high expression of MACC1 protein exhibited a poorer prognosis than those with low MACC1 expression. Furthermore, Cox multivariate analysis showed that MACC1 overexpression was an independent prognostic factor for predicting the overall survival of glioma patients. In conclusion, expression of MACC1 in glioma could be adopted as a candidate biomarker for the diagnosis of clinical stage and for assessing prognosis, indicating for the first time that MACC1 may play an important role in the tumor development and progression in glioma. MACC1 might be considered as a novel therapeutic target against this cancer.

Analyzing time-series microarray data reveals key genes in spinal cord injury.

Although many scholars have utilized high-throughput microarrays to delineate gene expression patterns after spinal cord injury (SCI), no study has evaluated gene changes in raphe magnus (RM) and somatomotor cortex (SMTC), two areas in brain primarily affected by SCI. In present study, we aimed to analyze the differentially expressed genes (DEGs) of RM and SMTC between SCI model and sham injured control at 4, 24 h, 7, 14, 28 days, and 3 months using microarray dataset GSE2270 downloaded from gene expression omnibus and unpaired significance analysis of microarray method. Protein-protein interaction (PPI) network was constructed for DEGs at crucial time points and significant biological functions were enriched using DAVID. The results indicated that more DEGs were identified at 14 days in RM and at 4 h/3 months in SMTC after SCI. In the PPI network for DEGs at 14 days in RM, interleukin 6, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), FBJ murine osteosarcoma viral oncogene homolog (FOS), tumor necrosis factor, and nuclear receptor subfamily 3, group C, member 1 (glucocorticoid receptor) were the top 5 hub genes; In the PPI network for DEGs at 3 months in SMTC, the top 5 hub genes were ubiquitin B, Ras-related C3 botulinum toxin substrate 1 (rho family, small GTP binding protein Rac1), FOS, Janus kinase 2 and vascular endothelial growth factor A. Hedgehog and Wnt signaling pathways were the top 2 significant pathways in RM. These hub DEGs and pathways may be underlying therapeutic targets for SCI.

Monitoring changes in quality of life in patients with lung cancer by using specialised questionnaires: implications for clinical practice.

BACKGROUND: Quality of life (QoL) in lung cancer patients is overlooked due to the severity of the disease. Changes in factors comprising QoL need further exploration to determine therapy targets. METHODS AND MATERIALS: QoL was assessed in 282 patients referred to a specialised centre in Greece for chemotherapy using three reliable scales: Functional Assessment of Cancer Therapy-Lung (FACT-L, Greek version 4), Short Form (SF-36) Health Survey and Hospital Anxiety and Depression Scale (HAD)S. RESULTS: Comparing QoL scores, it was observed that in comparison to the first chemotherapy, there was a statistically significant deterioration in patients' physical well-being (p < 0.0001) at the following chemotherapies. In contrast, there was a statistically significant improvement in patients' emotional well-being (p < 0.0001), mental health (p < 0.0001) and social functioning (p = 0.006) in the chemotherapies following the first. Observations deriving from survival analyses agree with literature findings: small cell lung cancer (SCLC) patients had significantly shorter survival than non-SLSC (NSCLC) patients, initial performance status was consistent with survival, radiotherapy improved survival, existence of metastases hindered survival, and the number of chemotherapies and QoL scores were positively correlated with survival. CONCLUSIONS: Although patients' physical functioning deteriorated after chemotherapy, their psychological state, mental health and social functioning improved in comparison with their first chemotherapy. This may be due to the fear of the unknown and the stress patients experience before their treatment. Regarding survival analysis results, it could be stated that the better QoL scores, the longer the survival. The findings underline the importance of psychological support after diagnosis and during the initiation of treatment. This may result in a better QoL, hence leading to prolongation of survival.

Selective bronchial occlusion for acquired bronchobiliary fistula caused by treatment of hepatocellular carcinoma: A case series.

Acquired bronchobiliary fistula (ABBF) is very rare among the complications that occur in patients with hepatocellular carcinoma (HCC) after treatment. Although surgery and drainage have been the main methods for treating ABBF for a long time, they are not entirely suitable for patients with refractory ABBF resulting from HCC therapy. In this study, we present four cases of ABBF caused by HCC treatment, who were treated using selective bronchial occlusion (SBO). Among the 4 patients with ABBF treated with SBO, 3 cases successfully blocked ABBF with SBO, and the treatment success rate was 75%. All successfully treated patients reported disappearance of symptoms of bilioptysis and cough was alleviated. No life-threatening adverse reactions were reported following SBO intervention, and no deaths occurred. We believe that the use of video bronchoscopy to place a self-made silicone plug in the bronchus to treat refractory ABBF is a feasible palliative treatment, which can significantly improve the condition of ABBF patients.